Transcriptional response of Pseudomonas aeruginosa PA3 to its phage gene product gp68
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ABSTRACT:
PROVIDER: PRJNA523578 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Explore the genome-scale influence of PA3 phage gene product gp68 on Pseudomonas aeruginosa PA3
2019-03-31 | GSE126873 | GEO
Project description:Explore the genome-scale phage–host interactions across different developmental infection stages Samples were taken from the PA3 Lysates infected with phage Pap3 at six internal time (0,5,10,20,30,80min). Three independent experiments were performed at each timme except for 80min without biological replicate.
2015-05-06 | E-GEOD-68584 | biostudies-arrayexpress
Project description:Explore the genome-scale phage–host interactions across different developmental infection stages
2015-05-06 | GSE68584 | GEO
Project description:Explore the genome-scale phage–host interactions across different developmental infection stages
2020-10-01 | GSE129181 | GEO
Project description:Transcriptional response of Pseudomonas aeruginosa PA3 to bacteriophage PaP3 infection
| PRJNA530399 | ENA
Project description:Quorum sensing (QS) is the cell density-dependent virulence factor regulator in Pseudomonas aeruginosa. Here, we elucidate PIT2, a phage-encoded inhibitor of the QS regulator LasR, derived from the lytic Pseudomonas phage LMA2. PIT2 inhibits the effectors PrpL and LasA of the type 2 secretion system of P. aeruginosa and attenuates bacterial virulence towards HeLa cells and in Galleria mellonella. Using RNAseq-based differential gene expression analysis, the effect of PIT2 on the LasR regulatory network was revealed. Moreover, the specific interaction between LasR and PIT2 was determined. These data expand our knowledge on phage-encoded modulators of the bacterial metabolism, as this examples an anti-virulence protein derived from a lytic phage. From an applied perspective, this phage protein reveals and exploits an interesting anti-virulence target in P. aeruginosa. As such, it lays the foundation for a new phage-inspired anti-virulence strategy to combat multidrug resistant pathogens and opens the door for SynBio applications.
2023-09-27 | GSE227677 | GEO
Project description:The ability of bacteriophages to kill bacteria is well known, as is their potential use as alternatives to antibiotics. As such, bacteriophages reach high doses locally through infection of their bacterial host in the human body. In this study we assessed the gene expression profile, by means of whole transcriptome analysis, of peripheral blood mononuclear cells (PBMCs) derived from a healthy human donor and stimulated with a Pseudomonas aeruginosa phage PNM lysate, or P. aeruginosa strain 573. The PBMCs were stimulated for 20 h, followed by lysis of the cells and RNA extraction. In total, three stimulations were performed: control sample (i.e. not stimulated), P. aeruginosa phage PNM lysate and P. aeruginosa strain 573. Each stimulation was conducted in triplicate. The transcriptome analysis showed that the phage induce a clear immunological responses. Both pro- and anti-inflammatory genes were up-regulated in the PBMCs in the presence of the phage or its bacterial host. Our results indicate that bacteriophages might play a bigger role in the immune response then previously described and might have a broader effect than the clearing of bacterial infections alone, such as the suppression of the immune response to benefit their own survival.
2017-03-02 | GSE95573 | GEO
Project description:The basic biology of bacteriophage–host interactions has attracted increasing attention due to a renewed interest in the therapeutic potential of bacteriophages. In addition, knowledge of the host pathways inhibited by phage may provide clues to novel drug targets. However, the effect of phage on bacterial gene expression and metabolism is still poorly understood. In this study, we tracked phage–host interactions by combining transcriptomic and metabolomic analyses in Pseudomonas aeruginosa infected with a lytic bacteriophage, PaP1. Compared with the uninfected host, 7.1% (399/5655) of the genes of the phage-infected host were differentially expressed genes (DEGs); of those, 354 DEGs were downregulated at the late infection phase. Many of the downregulated DEGs were found in amino acid and energy metabolism pathways. Using metabolomics approach, we then analyzed the changes in metabolite levels in the PaP1-infected host compared to un-infected controls. Thymidine was significantly increased in the host after PaP1 infection, results that were further supported by increased expression of a PaP1-encoded thymidylate synthase gene. Furthermore, the intracellular betaine concentration was drastically reduced, whereas choline increased, presumably due to downregulation of the choline–glycine betaine pathway. Interestingly, the choline–glycine betaine pathway is a potential antimicrobial target; previous studies have shown that betB inhibition results in the depletion of betaine and the accumulation of betaine aldehyde, the combination of which is toxic to P. aeruginosa. These results present a detailed description of an example of phage-directed metabolism in P. aeruginosa. Both phage-encoded auxiliary metabolic genes and phage-directed host gene expression may contribute to the metabolic changes observed in the host.
2018-05-03 | MTBLS431 | MetaboLights
Project description:It has been shown that the filamentous phage, Pf4, plays an important role in biofilm development, stress tolerance, genetic variant formation and virulence in Pseudomonas aeruginosa PAO1. These behaviours are linked to the appearance of superinfective phage variants. Here, we have investigated the molecular mechanism of superinfection as well as how the Pf4 phage can control host gene expression to modulate host behaviours. Pf4 exists as a prophage in PAO1 and encodes a homolog of the P2 phage repressor C. Through a combination of molecular techniques, ChIPseq and transcriptomic analyses, we show that repressor C (Pf4r) is the minimal factor for immunity against reinfection by Pf4 possibly through Pf4r binding to its putative promoter region, and that Pf4r also functions as a transcriptional regulator for expression of host genes. A binding motif for Pf4r was also identified. In wild type P. aeruginosa and Pfr4 complemented Pf4 deficient mutant strains, virulence factor related genes including phenazine and type VI secretion system effectors were upregulated, potentially explaining the reduced virulence of Pf4-deficient P. aeruginosa PAO1. X-ray crystal structure analysis shows that Pf4r forms symmetric homo-dimers homologous to the E.coli bacteriophage P2 RepC protein. A mutation associated with the superinfective Pf4r variant, found at the dimer interface, suggests dimer formation may be disrupted, which derepresses phage replication. This is supported by MALS analysis where the Pf4r* protein only shows monomer formation. Collectively, these data suggest the mechanism by which filamentous phages play such an important role in P. aeruginosa biofilm development.
2021-01-31 | GSE154459 | GEO
Project description:Two component systems (TCSs) control a large proportion of virulence factors in Pseudomonas aeruginosa. Yet, investigations on inhibitors of regulatory pathways of TCS remain scare, despite their potential in anti-virulence strategies. This work encompasses the working mechanism of PIT4, a protein derived from the lytic P. aeruginosa phage LSL4. This viral protein inhibits bacterial motility and in particular twitching motility, while reducing the virulence of P. aeruginosa towards HeLa cells. Via differential gene expression and a yeast two-hybrid screen, PIT4 was shown to interact with components of different two component systems. In one-on-one interaction assays, it was confirmed that PIT4 interacts with the histidine kinases FleS, PilS and PA2882, through interaction with the histidine kinase domain. As such, this work highlights the potential of previously unknown phage proteins in virulence regulation of multidrug resistant pathogens that might be exploited for anti-virulence strategies and biotechnological applications.
2023-09-25 | GSE230851 | GEO